Regulation of ydiV-induced biological characteristics permits Escherichia coli evasion of the host STING inflammatory response
文献类型: 外文期刊
作者: Wang, Xudong 1 ; Lin, Xinguang 1 ; Wan, Zhixin 1 ; Zuo, Jiakun 1 ; Wang, Zhihao 3 ; Xu, Yuanyuan 1 ; Phouthapane, Vanh 1 ;
作者机构: 1.Nanjing Agr Univ, Coll Vet Med, MOE Joint Int Res Lab Anim Hlth & Food Safety, Key Lab Anim Physiol & Biochem, Nanjing 210095, Peoples R China
2.Jiangsu Acad Agr Sci, Natl Res Ctr Vet Vaccine Engn & Technol China, Nanjing 210014, Peoples R China
3.Chinese Acad Agr Sci, Shanghai Vet Res Inst, Shanghai 200241, Peoples R China
4.Minist Sci & Technol MOST, Biotechnol & Ecol Inst, Viangchan, Laos
关键词: c-di-GMP; Biological characteristics; STING-IRF3 signaling pathway
期刊名称:VETERINARY MICROBIOLOGY ( 影响因子:3.293; 五年影响因子:3.599 )
ISSN: 0378-1135
年卷期: 2021 年 261 卷
页码:
收录情况: SCI
摘要: Mammary gland-derived Escherichia coli (E. coli) is an important pathogen causing dairy cow mastitis. YdiV, with EAL-like domains, inhibits flagellum biogenesis and motility and affects c-di-GMP (eubacterial signaling molecule) concentration changes in bacteria. However, the pathophysiological role of ydiV in host-pathogen cross-talk still needs to be elucidated. In this study, firstly constructed the ydiV mutant (NJ17 Delta ydiV) and ydiV complementary (cNJ17 Delta ydiV) E. coli strains to infect mouse mammary epithelial cells (EpH4-Ev) and macrophages (RAW264.7), as well as mouse mammary glands, respectively. Then biological characteristics, adaptor molecules in related signaling pathways, proinflammatory cytokines and the extent of host cell damage was evaluated. Compared with E. coli NJ17 infected mice, the bacterial load in the mammary gland of NJ17 Delta ydiV was significantly lower and the extent of the damage was alleviated. Notably, the deletion of ydiV significantly aggravated cell damage in RAW264.7 cells and compared with the wild-type strain, NJ17 Delta ydiV significantly activated the STING/TBK1/IRF3 pathway in macrophages. In EpH4-Ev cells, although STING did not sense E. coli NJ17 invasion, IRF3 was activated by the NJ17 Delta ydiV strain. Taken together, ydiV deletion significantly affects a variety of biological characteristics and induces severe cell damage, while the STING/TBK1/IRF3 pathway actively participated in pathogen elimination in the host. This study highlights a new role for ydiV in E. coli infection and provides a foundation for further studies to better understand host-bacteria interactions and potential prophylactic strategies for infectious diseases.
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